Weisshorn R, Wappler F, Fiege M, Gerbershagen M, Schulte Am Esch J
Klinik und Poliklinik für Anästhesiologie, Universitätsklinikum Hamburg-Eppendorf.
Anasthesiol Intensivmed Notfallmed Schmerzther. 2002 Mar;37(3):138-43. doi: 10.1055/s-2002-21806.
The abuse of cocaine can cause serious medical complications like tachycardia, rhabdomyolysis, and hyperthermia. Because of the clinical similarities, it has been suggested that cocaine might be a trigger of malignant hyperthermia (MH). Therefore, aim of this study was to investigate the in-vitro effects of cocaine in skeletal muscle specimens of MH susceptible (MHS) and normal (MHN) patients.
62 patients undergoing the in-vitro contracture test (IVCT) according to the protocol of the European MH Group (EMHG) for diagnosis of MH susceptibility were included in this study. In muscle specimens surplus to diagnostic requirements cocaine was added in order to achieve tissue bath concentrations of 0.01, 0.1 and 1.0 mM. The contracture development and twitch response have been registered.
21 patients were diagnosed as MHS and 36 patients as MHN. 5 patients tested as MH-equivocal (MHE) were excluded from the study. Following bolus administration of cocaine, no contracture development was observed in MHS, as well as MHN specimens. The muscle twitch decreased after cocaine administration significantly in both diagnostic groups.
In contrast to the established MH trigger substances like volatile anaesthetics, cocaine produced no contracture development in MHS muscle specimens. Furthermore, cocaine produced a negative inotropic effect in all skeletal muscle preparations, which might be explained by local anaesthetic effects. Regarding these results, cocaine seems not to be a MH trigger agent.
可卡因滥用可导致严重的医学并发症,如心动过速、横纹肌溶解和高热。由于临床症状相似,有人提出可卡因可能是恶性高热(MH)的诱发因素。因此,本研究旨在调查可卡因对MH易感(MHS)患者和正常(MHN)患者骨骼肌标本的体外作用。
本研究纳入了62例根据欧洲MH小组(EMHG)方案进行体外挛缩试验(IVCT)以诊断MH易感性的患者。在诊断所需的多余肌肉标本中加入可卡因,以使组织浴浓度达到0.01、0.1和1.0 mM。记录挛缩发展情况和抽搐反应。
21例患者被诊断为MHS,36例患者被诊断为MHN。5例检测结果为MH可疑(MHE)的患者被排除在研究之外。在推注可卡因后,MHS和MHN标本中均未观察到挛缩发展。在两个诊断组中,可卡因给药后肌肉抽搐均显著降低。
与挥发性麻醉剂等已确定的MH诱发物质不同,可卡因在MHS肌肉标本中未引起挛缩发展。此外,可卡因在所有骨骼肌制剂中均产生负性肌力作用,这可能由局部麻醉作用来解释。基于这些结果,可卡因似乎不是MH诱发剂。